MicroRNA-190b inhibits tumor cell proliferation and induces apoptosis by regulating Bcl-2 in U2OS osteosarcoma cells

Osteosarcoma (OS) is one of the most prevalent malignancies in bone with no established therapy so far. This study was aimed to clarify the role of miR-190b in tumor cell growth of OS. The nniR-190b mimic, inhibitor and miR-control were transfected into human OS U2OS cells. Then U2OS cell proliferation was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MU) and bromodeoxyuridine (BrdU) incorporation assay. The apoptotic U2OS cells were detected by flow cytometry. Additionally, cell-cycle regulators p27, p21 and apoptosis factors B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X (Bax), caspase-3 were examined by western blotting. Overexpressing miR-190b observably reduced cell viability, BrdU-positive cells (both P < 0.05) and caused strong accumulation of cell-cycle inhibitor p27 in U2OS cells compared with the miR-control, whereas the miR-190b inhibitor exerted opposite effects. Further, a marked increase of 18% rate of apoptotic cells by the overexpressing miR-190b (P < 0.01) and 4% decrease by miR-190b inhibitor (P < 0.05) were detected. The protein expressions of BcI-2 were downregulated, Bax, pro-caspase-3 and active caspase-3 were upregulated by overexpressing miR-190b in U2OS cell line, while miR-190b inhibitor achieved opposite effects. The present study demonstrates that miR-190b inhibits tumor cell proliferation and induces apoptosis by regulating BcI-2 in U2OS cells, which points to miR-190b as a novel oncosuppressor for OS. The identified tumor suppressive capacity of miR-190b provides novel avenues for achieving better OS therapy.